Objective:To explore the effects and mechanism of Hu Qi San on carbon tetrachloride ( CC14 ) induced hepatic fibrosis in rats. Methods:After establishing the liver fibrosis rat model by intraperitoneal injection of CC14, Hu Qi San were given by oral administration. Liver tissue and blood were harvested after 4 weeks of intervention by Hu Qi San, which were detected by RIA, HE, Mallory, PCNA and TUNEL Results:Compared with model group, the levels of serum Col I were significantly decreased in positive drugs (Gan Pi Kang) group and high dose of Hu Qi San treattment group (P <0.05) . Moreover, the levels of LN in serum were significantly decreased in low dose of Hu Qi San treatment group ( P < 0. 05) . The histopathological results showed there were alleviated changes in hepatic tissue treated by Hu Qi San and Gan Pi Kang. Immunohistochemical results showed that the positive cells of PCNA were decreased and apoptotic cells were increased significantly. Conclusion:Hu Qi San shows great effect of anti-liver fibrosis. The initial mechanisms are regarded as inhibiting the proliferation and promoting the apoptosis of hepatic cells in liver fibrotic tissue.%目的:观察槲芪散抗四氯化碳(CCl4)诱发大鼠肝纤维化的疗效,初步探讨该药对肝细胞增殖和凋亡的影响.方法:腹腔注射“CCl4-橄榄油”混悬液制备大鼠肝纤维化模型；槲芪散(高、低两个剂量)灌胃给药,治疗时间4周；放免法测定大鼠血清中Ⅰ型胶原(Col Ⅰ)、透明质酸(HA)、层粘连蛋白(LN)及纤粘连蛋白(FN)的含量,肝组织石蜡切片进行HE、Mallory、TUNEL(缺口末端标记技术)及增殖细胞核抗原(PCNA)免疫组织化学显色.结果:肝纤维化大鼠血清中Col Ⅰ、HA、LN、FN含量均显著升高(P＜0.05)；阳性对照药(肝脾康)、槲芪散高剂量治疗组大鼠血清Col Ⅰ及槲芪散低剂量治疗组大鼠血清LN的含量显著下降(P＜0.05)；而HA及FN含量未见明显改变.组织病理学检测可见,肝脾康及槲芪散治疗组大鼠肝组织胶原含量显著减少、病理程度显著减轻；免疫组化结果显示肝脾康及槲芪散治疗组大鼠肝组织增殖细胞减少、凋亡细胞显著增多.结论:槲芪散抗实验性肝纤维化药效显著,其初步药理机制是抑制肝组织内细胞外基质的过度合成,抑制肝细胞的过度增殖,促进肝细胞的凋亡.
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